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LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-ß/Smad signaling via miR-424-5p.
Huan, Qing; Cheng, Shu-Chao; Du, Zhan-Hui; Ma, Hui-Fen; Li, Cheng.
Afiliación
  • Huan Q; Reproductive Center, The First People's Hospital of Yueyang (Central South University, Xiangya School of Medicine, Yueyang Clinical College), Yueyang, China.
  • Cheng SC; Office of Invitation to Bid, The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China.
  • Du ZH; Heart Center, Qingdao Women and Children's Hospital, Qingdao University, Qingdao, China.
  • Ma HF; National Health Commission Capacity Building and Continuing Education Center, Beijing, China.
  • Li C; Reproductive Center, The First People's Hospital of Yueyang, Yueyang, China.
J Obstet Gynaecol Res ; 47(7): 2394-2405, 2021 Jul.
Article en En | MEDLINE | ID: mdl-33949053
AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-ß1 (TGF-ß1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-ß/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: MicroARNs / Endometriosis / ARN Largo no Codificante Tipo de estudio: Prognostic_studies Límite: Female / Humans Idioma: En Revista: J Obstet Gynaecol Res Asunto de la revista: GINECOLOGIA / OBSTETRICIA Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: MicroARNs / Endometriosis / ARN Largo no Codificante Tipo de estudio: Prognostic_studies Límite: Female / Humans Idioma: En Revista: J Obstet Gynaecol Res Asunto de la revista: GINECOLOGIA / OBSTETRICIA Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia